Rotator cuff tendon tears are a widespread orthopedic problem that often requires surgical repair to eliminate pain and restore function. The success of the surgical repair has been mixed, with a large percentage of patients suffering from re-tears due to failed healing and other complications, such as joint stiffness. Type II diabetes mellitus is one condition that has substantially increased over the past decade and is linked with altered tissue properties, poor healing and joint stiffness, which are hallmark characteristics of rotator cuff repair patients. Unfortunately, limited research exists examining how diabetes affects the complex tendon healing response and the mechanics of the joint. One recent study in a type I diabetic rat model determined that following rotator cuff tendon repair there are considerable deficits in tendon mechanical properties during the early stages of healing. Although this study highlighted the mechanical changes that could occur specifically with tendon healing in the presence of hyperglycemia, it does not address the altered tissue properties, biologic mechanisms, and the restricted joint motion that occur, nor did it address the most common form of diabetes. The use of our laboratory's well established in vivo rat model of supraspinatus tendon tears and the extensively used Goto-Kakizaki rat as a model for type II diabetes allows for the direct examination of the mechanisms that cause altered tissue properties and decreased tendon healing in this disease state, which would otherwise be impossible to study in the human. With the combination of these two well established animal models, the overall objectives of this study are to determine the mechanisms that lead to alterations in uninjured tendon properties and detrimental tendon healing caused by type II diabetes. Our global hypothesis is that type II diabetes will cause increased and prolonged biological mediators that will disrupt the normal uninjured properties of the tendon and progression of tendon healing. Our specific aims are: Specific Aim 1: To compare shoulder joint mechanics and tendon properties (mechanics, gene expression, protein content) of healthy and type II diabetic rats; and Specific Aim 2: To determine the effect of type II diabetes on shoulder joint mechanics and rotator cuff tendon healing (mechanics, gene expression, and protein content) following an acute rotator cuff tear. These analyses will provide insight into the complex processes of rotator cuff tendon homeostasis and repair response to injury that are affected by type II diabetes and how they relate to functional limitations. The results of this study will provide the framework for future studies that will attempt to therapeutically augment the deleterious cascade of biologic mediators seen in type II diabetes. Ultimately, this will provide physicians with further tools for efficiently treating patients with type II diabetes that are suffering from tendon injuries.